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In areas where rheumatic fever is still prevalent, particularly in poor and crowded inner-city populations where medical care is episodic, follow-up may be lacking, and compliance in taking oral penicillin cannot be relied on, treatment with intramuscular penicillin Gbenzathine remains preferred [11].

Anti-streptococcal antibodies cross-reactive with N-acetyl-betaD-glucosamine (GlcNAc) and myosin are present in the sera of patients with rheumatic fever (RF) [13].

The story of the prevention of rheumatic fever has a large cast of characters, but special recognition must be given to Coburn for his observations confirming the role of the hemolytic streptococcus published in 1931 and showing the prophylactic value of sulfanilamide published in 1939 [15].

Molecular mimicry or epitope similarity between group A streptococcal M proteins and myosin may contribute to the presence of heart reactive antibodies in acute rheumatic fever[5].

In conclusion, it was found that exposure to pharyngeal infection with group A beta haemolytic streptococci may lead to acute rheumatic fever in those with an inherited recessive gene responsible for high responsiveness to the streptococcal polysaccharide antigen of the cell wall[17].

The aim of the present study was to evaluate the DNA damage in children receiving one dose of 1.2 million units benzathine penicillin every 4 weeks over a long period to prevent recurrences of rheumatic fever[19].

METHODS: Echocardiography and assessment of cardiac troponin I (cTnI) blood levels were systematically performed in 95 consecutive patients with acute rheumatic fever, who were divided into three groups [28].

The occurrence of IgE and IgG antibodies to penicillin G and V in children on long-term treatment with penicillin as secondary prophylaxis for rheumatic fever was studied using Phadebas RAST (Pharmacia Diagnostics, Uppsala, Sweden) and ELISA respectively [30].